The most complete genetic study to date of the SARS virus has revealed an agent that appears to undergo almost negligible mutation, a phenomenon that is described as "a double-edged sword" for the scientists battling to eradicate it.

In research published online this week by The Lancet, a team of scientists led by Dr Edison Liu from the Genome Institute of Singapore compared the genetic identity of samples of Severe Acute Respiratory Syndrome (SARS) virus, taken in throat swabs from local patients, with the genome of samples found in other countries.

The most important areas of the genomes were identical, something that is remarkable in so-called RNA viruses, which includes SARS and other members of the coronavirus family. Usually, RNA viruses mutate very quickly, changing a letter or so in their genetic code every time they replicate.

This evolution is part of the virus' drive to survive, perhaps finding ways of evading the defence mechanisms of its host or of transferring to a new and more profitable host. Liu and colleagues sequenced the genetic code of a SARS virus taken from one of the first known carriers of the disease, and of SARS viruses found in four people in Singapore who had had direct or secondary contact with that individual. These sequences were compared with virus isolates from Canada, Hanoi and Hong Kong and from Guangzhou and Beijing in China.

The 14 sequences contained small signatures that pointed to where they originated - something that could be a useful epidemiological tool - but there was no major variant in their genetic machinery.

SARS may be here to stay

In a commentary also published by The Lancet, molecular biologists Dr Earl Brown and Jason Tetro from the University of Ottawa, Canada, said that Liu's evidence pointed to "a remarkable genetic conservation" of the virus since the outbreak was first documented in February.

"This finding may be a double-edged sword," they warned. It shows that the virus is well adapted to lodging in the human host - in other words, there is the risk that it is here to stay. The virus is not under significant threat from the immune system and so has no need to mutate to a different - possibly more benign - form. Mutation such as this is what causes flu epidemics to die out.

On the other hand, the SARS virus' relative stability should make it easier to target it with a vaccine, they said. Viruses that mutate quickly - cold, flu and to a lesser degree HIV are among them - are in effect a moving target, because vaccines work by teaching antibodies and killer blood cells the face of a familiar enemy.

Brown added a caveat. Vaccines to combat animal versions of the coronavirus have had only limited success. "We're not sure why this is. It could be that the virus changes shape in response to the vaccine and ducks the immune system."

SARS has killed more than 500 people and infected over 7,300 since it first emerged in China late last year. Still to come are answers to other big unknowns: exactly how the virus is transmitted; why some people are more vulnerable or more infectious than others; and, of course, where are the weak points in the virus which can be exploited by drugs and vaccines.